Regulation of IgE production from human mononuclear cells by beta 2-adrenoceptor agonists

Clin Exp Allergy. 1995 Apr;25(4):304-11. doi: 10.1111/j.1365-2222.1995.tb01047.x.


The present study examined the effect of beta 2-adrenoceptor agonists on the interleukin-4 (IL-4)-driven IgE production and on the possible mechanisms of action of these compounds. We present evidence that salbutamol and fenoterol potentiated the IL-4-induced IgE production by human peripheral blood mononuclear cells (PBMC). No significant effect of incubation in the presence of beta 2-adrenoceptor agonists on IgG, IgA and IgM production was observed. Salbutamol and fenoterol inhibited interferon-(IFN)-gamma production by PHA-activated human PBMC suggesting that the blockade of the production of this cytokine could possibly explain the enhancement of IgE production. Salbutamol and fenoterol potentiated the IL-4-induced production of sCD23 whereas no effect on CD23 expression was observed. The potentiating effect of salbutamol on IgE production was blocked by two antagonists of beta 2-adrenoceptor, namely butoxamine and D,L-propranolol, suggesting a beta-adrenoceptor-mediated event. These results demonstrate that beta 2-adrenoceptor stimulation results in an increase in IgE production by human B lymphocytes.

MeSH terms

  • Adrenergic beta-Agonists / pharmacology*
  • Albuterol / pharmacology
  • Cell Survival / drug effects
  • Humans
  • Immunoglobulin E / biosynthesis*
  • Immunoglobulins / blood
  • Interleukin-4 / pharmacology
  • Lymphocyte Activation / drug effects
  • Lymphokines / blood
  • Monocytes / metabolism*
  • Receptors, Adrenergic, beta / physiology
  • Receptors, IgE / metabolism
  • Solubility


  • Adrenergic beta-Agonists
  • Immunoglobulins
  • Lymphokines
  • Receptors, Adrenergic, beta
  • Receptors, IgE
  • Interleukin-4
  • Immunoglobulin E
  • Albuterol